miR-26b Mimic Inhibits Glioma Proliferation In Vitro and In Vivo Suppressing COX-2 Expression
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Updated: Feb 24, 2026
Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
Zheng-Gang Chen1, Chuan-Yi Zheng1, Wang-Qing Cai2
1Department of Neurosurgery, The First Affiliated Hospital of Hainan Medical College, Haikou, Hainan, P.R. China.
Abstract:
Glioma is the most common malignant tumor of the nervous system. Studies have shown the microRNA-26b (miR-26b)/cyclooxygenase-2 (COX-2) axis in the development and progression in many tumor cells. Our study aims to investigate the effect and mechanism of the miR-26b/COX-2 axis in glioma. Decreased expression of miR-26b with increased levels of COX-2 was found in glioma tissues compared with matched normal tissues. A strong negative correlation was observed between the level of miR-26b and COX-2 in 30 glioma tissues. The miR-26b was then overexpressed by transfecting a miR-26b mimic into U-373 cells. The invasive cell number and wound closing rate were reduced in U-373 cells transfected with miR-26b mimic. In addition, COX-2 siRNA enhanced the effect of miR-26b mimic in suppressing the expression of p-ERK1 and p-JNK. Finally, the in vivo experiment revealed that miR-26b mimic transfection strongly reduced the tumor growth, tumor volume, and expression of matrix metalloproteinase-2 (MMP-2) and MMP-9. Taken together, our research indicated a miR-26b/COX-2/ERK/JNK axis in regulating the motility of glioma in vitro and in vivo, providing a new sight for the treatment of glioma.
Insights
MicroRNA-26b (miR-26b) suppresses glioma progression by targeting cyclooxygenase-2 (COX-2). This study reveals a miR-26b/COX-2 pathway regulating glioma cell motility and tumor growth, offering new therapeutic strategies.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cancer Research
Background:
- Glioma is a prevalent and aggressive nervous system malignancy.
- The microRNA-26b (miR-26b)/cyclooxygenase-2 (COX-2) axis is implicated in various tumor progressions.
- Understanding the miR-26b/COX-2 axis in glioma is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role and mechanism of the miR-26b/COX-2 axis in glioma.
- To evaluate the therapeutic potential of modulating this axis in glioma treatment.
Main Methods:
- Analysis of miR-26b and COX-2 expression in glioma tissues.
- In vitro studies using U-373 cells with miR-26b mimic and COX-2 siRNA transfection.
- In vivo experiments assessing tumor growth following miR-26b mimic transfection.
Main Results:
- Glioma tissues showed decreased miR-26b and increased COX-2 expression, with a negative correlation between them.
- Overexpression of miR-26b reduced glioma cell invasion and migration in vitro.
- The miR-26b mimic suppressed tumor growth, volume, and matrix metalloproteinase expression in vivo.
- The miR-26b/COX-2 pathway influenced ERK and JNK signaling.
Conclusions:
- A novel miR-26b/COX-2/ERK/JNK axis regulates glioma cell motility both in vitro and in vivo.
- Targeting the miR-26b/COX-2 axis presents a promising therapeutic strategy for glioma.
